Metabolic Acidosis Medications

High Anion Gap Metabolic Acidosis

When acidosis is present on blood tests, the first step in determining the cause is determining the anion gap. If the anion gap is high (>12 mEq/L), there are several potential causes. High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). An anion gap is usually considered to be high if it is over 12 mEq/L. High anion gap metabolic acidosis is caused generally by acid produced by the body,. More rarely, high anion gap metabolic acidosis may be caused by ingesting methanol or overdosing on aspirin.[1][2] The Delta Ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether mixed acid base disorder (metabolic acidosis) is present. The list of agents that cause high anion gap metabolic acidosis is similar to but broader than the list of agents that cause a serum osmolal gap. Causes[edit] Causes include: The newest mnemonic was proposed in The Lancet reflecting current causes of anion gap metabolic acidosis:[3] G — glycols (ethylene glycol & propylene glycol) O — oxoproline, a metabolite of paracetamol L — L-lactate, the chemical responsible for lactic acidosis D — D-lactate M — methanol A — aspirin R — renal failure K — ketoacidosis, ketones generated from starvation, alcohol, and diabetic ketoacidosis The mnemonic MUDPILES is commonly used to remember the causes of increased anion gap metabolic acidosis.[4][5] M — Methanol U — Uremia (chronic kidney failure) D — Diabetic ketoacidosis P — Paracetamol, Propylene glycol (used as an inactive stabilizer in many medications; historically, the "P" also stood for Paraldehyde, though this substance is not commonly used today) I — Infectio
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Metabolic Acidosis Due To Drugs And Toxins

3.1.4.7.Metabolic Acidosis due to Drugs and Toxins Metabolic Acidosis due to Drugs and Toxins Several drugs and toxins have been implicated as direct or indirect causes of a high-anion gap metabolic acidosis (HAGMA). A consideration of these drugs needs to be included in an differential diagnosis of a HAGMA. The three most common ones to consider are methanol, ethylene glycol and salicylates. Other toxins which can cause acidosis are isopropyl alcohol and butoxyethanol. Toluene also causes an acidosis and the anion gap may be normal or elevated. * Initially no acid-base disorder due to long latent period while methanol is metabolised * Later, typically develop a high anion gap metabolic acidosis -due to formic acid * May also develop a respiratory acidosis secondary to CNS depression (with depression of respiratory centre and/or airway obstruction) * May occasionally present with normal anion gap acidosis if smaller ingestion * If patient is an alcoholic, there may other types of acidosis present as well (eg alcoholic ketoacidosis, starvation ketoacidosis, lactic acidosis, respiratory acidosis due aspiration, respiratory alkalosis due chronic liver disease.) Principles of Treatment of Methanol Poisoning Resuscitation: Airway, Breathing, Circulation. Obtunded patients require intubation for airway protection and ventilation. Haemodialysis is the most effective technique; it also removes ethanol so ethanol infusion rate must be increased during periods of dialysis This involves competitive inhibition of alcohol dehydrogenase (ADH). The aim is to delay the production of the toxic metabolites and limit the peak concentrations achieved. Two agents are currently in use: * Ethanol: "Ethanol blocking" treatment is the traditional treatment but has the disadvantage of causing i
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Drug-induced Metabolic Acidosis

Pharmacologically-Induced Metabolic Acidosis. Liamis G et al. Drug Saf 2010 May 1; 33:371-391. This somewhat wordy article is a complete review of drug-induced metabolic acidosis, and well worth reading for those interested in expanding their knowledge beyond the mnemonic MUDPILES or reviewing the 4 types of renal tubular acidosis. There is so much detail here that the paper is impossible to summarize, but here are some of its clinical pearls: Most of the patients who develop metformin-associated lactic acidosis had been taking the drug despite have a contraindication to its use, such as renal insufficiency or severe underlying disease. Antiviral therapy, especially nucleotide reverse transcriptase inhibitors, have been associated with life-threatening metabolic acidosis. Drugs implicated most often include didanosine, stavudine, and zidovudine. Linezolid impairs mitochondrial function and can cause metabolic acidosis, usually after prolonged therapy. The occurrence of metabolic acidosis in patients on propofol may herald onset of propofol infusion syndrome , which has a mortality rate of greater than 80%. Occult laxative abuse is on the differential diagnosis for a patient with unexplained hyperchloremic metabolic acidosis.
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Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... As previously stated, sodium bicarbonate (NaHCO3) is the agent most commonly used to correct metabolic acidosis. Also as previously mentioned, the role of alkali therapy is controversial in the treatment of lactic acidosis, with some evidence suggesting that HCO3- therapy produces only a transient increase in the serum HCO3- level and that this can lead to intracellular acidosis and worsening of lactic acidosis. Acute metabolic acidosis is usually treated with alkali therapy to raise plasma pH and to maintain it at greater than 7.20. THAM combines with hydrogen ions to form a bicarbonate buffer. It is used to prevent and correct systemic acidosis. It is available as 0.3-mol/L IV solution containing 18 g (150 mEq) per 500 mL (0.3 mEq/mL). This agent is used in the treatment of salicylate poisoning. It reduces the reduction of hydrogen ion secretion at the renal tubule and increases excretion of sodium, potassium, bicarbonate, and water. The goal is to maintain the urine pH at greater than 7.5 until the salicylate level falls below 30-50 mg/dL. These agents are used for the treatment of ketoacidosis. Insulin is administered, to facilitate cellular uptake of glucose, reduce gluconeogenesis, and halt lipolysis and production of ketone bodies. In addition, normal saline is administered to restore extracellular volume; potassium and phosphate replacement also may be necessary. This agent can be used to increase the excretion of salicylate. It is used in the emergency treatment of poisoning caused by drugs and chemicals. The network of pores present in activated charcoal absorbs 100-1000 mg of drug per gram of charcoal. It prevents absorption by adsorbing the drug in the intestin
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Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol
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Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment of Acidosis: Sodium Bicarbonate and Other Drugs Lactic acidosis, defined as a lactate level > 5 mmol/1 and a pH 7.35, is far and away the most-important acidosis during critical illness and most of this discussion of acidosis treatment will focus on treatment of lactic acidosis. Even in the face of maximal supportive therapy, lactic acidosis is associated with a mortality of 60-90% [ 1 , 2 , 3 , 4 ], so physicians have long relied on treatments to lower the [H+], such as sodium bicarbonate. Less common than lactic acidosis, and much more amenable to conventional treatments, are ketoacidoses and respiratory acidosis, but these too occasionally prompt consideration of alkalinizing therapies. Lowering the [H+] in blood depends on manipulating the strong ion difference ([SID]), total concentration of non-volatile weak acid buffer (ATOT), or arterial CO2 tension (PaCO2), or raising the total concentration of weak bases, BTOT (normally sufficiently small that it can be ignored). Therefore, potential treatments include: 1. Raise [SID]: a) add strong cations: bicarbonate, carbicarb, dialysis b) remove strong anions: dichloroacetate (DCA), dialysis, thiamine, riboflavin, vasoactive drugs? 2. Lower the paCO2: raise VE or lower VD/VT or VCO2 3. Reduce ATOT: remove albumin, but very limited effect Acute Lung InjurySodium BicarbonateAcute Respiratory Distress SyndromeLactic AcidosisDiabetic Ketoacidosis These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Weil MH, Afifi AA (1970) Experimental and clinical studies on lactate and pyruvate as indicators of th
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Toxin-induced Metabolic Acidosis

Acid-base disorders, poisoning, toxic, toxins, overdose, metabolic acidosis, acidosis, anion gap metabolic acidosis, strong ion gap acidosis Metabolic acidosis is a common and serious presentation of several toxins. Toxin-induced metabolic acidosis can be due to multiple diverse pathways and can become become evident at various stages and time-frames of the poisoning. These include organic acid production through metabolic pathways, exogenous acid addition, tissue hypoperfusion, renal impairment and cytopathic pathways. These variable pathways and presentations make the diagnosis and treatment challenging, and when a poisoning is suspected, consultation with a regional poison center and toxicologist is hightly recommended. There are numerous toxins that produce acid-base disturbances; however, we will only discuss the most common and serious toxins that result in a metabolic acidosis. The clinical features of metabolic acidosis are similar regardless of the etiology. Depending on the toxin, type and amount of exposure, there may be other specific clinical features. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Hyperventilation (rapid shallow or Kussmaul respirations). Chest pain, cardiac dysrhythmias, palpations. Many poisoned patients are unable to provide a reliable history; therefore, laboratory and other ancillary testing is essential. Some patients will present with classic toxidromes (e.g. opioid, anticholinergic, cholinergic or sympathomimetic), others will have family or friends relay important information regarding recent activity and possible exposure. To adequately assess these patients, it is essential to use a systematic approach, as many different poisons will have subtle overlapping signs and symptoms. Mana
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Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid
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Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche
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Drug And Chemical-induced Metabolic Acidosis.

Abstract Metabolic acidosis produced by drugs and/or chemicals can be conveniently divided into those with an increase in the anion gap (anion gap = Na- (Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and beta-hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed.
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List Of Metabolic Acidosis Medications (10 Compared) - Drugs.com

Adequate and well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters). Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in pregnant women. Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use in pregnant women despite potential risks. There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use in pregnant women despite potential risks. Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use in pregnant women clearly outweigh potential benefits. Is not subject to the Controlled Substances Act. Has a high potential for abuse. Has no currently accepted medical use in treatment in the United States. There is a lack of accepted safety for use under medical supervision. Has a high potential for abuse. Has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions. Abuse may lead to severe psychological or physical dependence. Has a potential for abuse less than those in schedules 1 and 2. Has a currently accepted medical use in treatment in the United States. Abuse may lead to moderate or low physical dependence or high psychological dependence. Has a low potential for abuse relative to those in schedule 3. It has a
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Popular Drugs Used To Treat Metabolic Acidosis - Goodrx

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